Genome-scale CRISPR screening for potential targets of ginsenoside compound K.
Yuanyuan YangXiaojian LiuShuang LiYanhao ChenYongxu ZhaoYuda WeiYan QiuYan LiuZhihua ZhouJun HanGuohao WuQiurong DingPublished in: Cell death & disease (2020)
Ginsenosides exhibit a large variety of biological activities in maintaining physical health; however, the molecule underpinnings underlining these biological activities remain to be defined. Here, we took a cellular condition that compound K (CK) induces autophagic cell death in HeLa cells, and setup a high-throughput genetic screening using CRISPR technology. We have identified a number of CK-resistant and CK-sensitive genes, and further validated PMAIP1 as a CK-resistant gene and WASH1 as a CK-sensitive gene. Compound K treatment reduces the expression of WASH1, which further accelerates the autophagic cell death, highlighting WASH1 as an interesting downstream mediator of CK effects. Overall, our study offers an easy-to-adopt platform to study the functional mediators of ginsenosides, and provides a candidate list of genes that are potential targets of CK.
Keyphrases
- cell death
- genome wide
- protein kinase
- cell cycle arrest
- high throughput
- dna methylation
- copy number
- genome wide identification
- crispr cas
- public health
- mental health
- healthcare
- genome editing
- poor prognosis
- physical activity
- human health
- oxidative stress
- induced apoptosis
- cell proliferation
- genome wide analysis
- combination therapy
- binding protein
- climate change
- long non coding rna
- replacement therapy